SARS患者CD4~+T细胞水平与胸部X线表现的动态变化研究

为探讨SARS患者的CD4 + T淋巴细胞改变与胸部X线表现及临床表现的动态变化关系 ,为SARS的诊断治疗提供相应依据。 (1)通过每天测体温 ,了解热度、热程以及发热规律 ;(2 )入院后行CD4 + T淋巴细胞计数检测 ,此后每隔 2～ 3d进行一次 ;(3)每隔 2 4～ 72h摄胸部正侧位片。结果 2 3例均有发热 ,37 8～ 4 0 1℃。重症患者热程 (12 82± 4 4 9)d ;普通患者为 (7 6 0± 3 14 )d ,(P <0 0 5 )。入院初CD4 + T细胞平均为 17 9%± 5 6 % ;治疗 15～ 30d后为 2 9 4 %± 5 4 %。高峰期CD4 + T细胞最低 12 5 %± 6 2 % ,与其他各期比较 ,差异有显著性意义 (P <0 0 1) ;恢复期 5例肺纤维化患者CD4 + T细胞为2 2 4 %± 4 8% ,较 18例无肺纤维化患者 31 4 %± 4 4 %明显降低 (P <0 0 1) ;5例并发肺纤维化患者恢复时间 (35 8± 12 5 )d ,较 18例无肺纤维化患者 (2 5± 8 6 )d明显延长 (P <0 0 1)。通过CD4 + T细胞和胸部X线的动态观察 ,两者基本呈平行变化 ,但CD4 + T细胞降低较胸部X线改变发生早 ,恢复时间较晚 ,且与肺纤维化的形成有关     

肾移植患者T淋巴细胞核仁组织区嗜银蛋白的监测

目的　研究外周血T淋巴细胞核中的rDNA转录活性在异体肾移植手术前后的变化及其敏感性。方法　异体肾移植手术前后取外周血T淋巴细胞 ,检测核仁银染面积与核面积的比值(Ag NORs) ,同时取血做T淋巴细胞表面抗原测定和病毒抗体检测。结果　外周血T淋巴细胞Ag NORs含量由术前的 (6 2 9± 0 97) % ,分别下降为术后 1周的 (4 6 3± 0 90 ) % ,术后 2周的 (4 81±1 6 ) %和术后 3周的 (4 5 6± 1 2 ) %。手术前的Ag NORs值与术后不同时期的Ag NORs值比较差异有显著性 (P <0 0 5 )。术后不同时期的Ag NORs值之间差异无显著性 (P >0 0 5 ) ;Ag NORs值不受性别及有无病毒感染的影响。T淋巴细胞表面抗原测定 ,CD3、CD4、CD8、CD4/CD8等手术前后无显著性变化 ,也不受病毒感染的影响。结论　外周血T淋巴细胞Ag NORs值可用于肾移植患者的免疫监测 ;在免疫低下人群中用Ag NORs值监测免疫状态较T淋巴细胞表面抗原测定敏感。     

rhIL-11和rhG-CSF联合应用对小鼠外周血T细胞亚群比例影响

为观察rhIL 11联合rhG CSF动员小鼠外周造血干细胞时 ,外周血T细胞亚群的变化 ,使用rhIL 11联合rhG CSF动员C5 7BL/ 6小鼠外周造血干细胞 ,观察用药不同时间小鼠外周血白细胞变化 ,同时通过流式细胞仪测定外周血T细胞亚群的变化。结果发现 ,小鼠注射rhIL 11后 ,外周血WBC明显升高 (P =0 0 0 3) ;单独注射rhG CSF或联用rhIL 11后 ,外周血WBC于第 5天达峰值 ,分别由用药前的 (7 5 3± 1 6 5 )× 10 9/L、 (7 2 7± 1 4 8)× 10 9/L上升至 (2 7 12± 1 84 )× 10 9/L、 (2 8 98± 3 13)× 10 9/L ,均显著高于对照组 (P值均为 0 0 0 1) ,而rhG CSF组与联合组之间无显著性差异 (P >0 0 5 )。CD3+ 细胞比例在用药组均高于正常对照组 (P值均 <0 0 5 ) ,rhIL 11组CD3+ 细胞及CD4 + 细胞比例逐渐增高 ,于动员的第 5天达峰值 (P值均为 0 0 0 1) ,CD8+ 细胞的比例没有明显变化 (P >0 0 5 ) ;在rhG CSF组CD3+ 细胞也有明显增高 ,并于动员第五天达峰值 (P =0 0 0 1) ,CD4 + 细胞的比例没有明显变化 (P值均 >0 0 5 ) ,但CD8+ 细胞的比例明显升高 (P =0 0 0 1) ;在联合组中CD3+ 、CD4 + 、CD8+ 细胞的比例变化均有明显升高。结果证明 ,rhIL 11联合rhG CSF能明显提高外周血WBC ,增加CD3+ 细胞比例 ,同时rhIL 11     

肾移植急性排斥反应时B7-2/CD28信号通路的表达*☆

背景：以往动物研究表明,在器官移植急性排斥反应时共刺激分子的表达与急性排斥反应密切相关。 目的：观察急性排斥反应时患者移植肾脏组织和外周血中B7-2/CD28信号通路的表达。 方法：对53例同种异体肾移植患者于移植前1 d、移植后1,3,7,14,21,28 d分别取外周血以及在临床诊断急性排斥反应当天和抗排斥治疗1周后额外采血,用流式细胞仪检测共刺激分子B7-2/CD28在外周血淋巴细胞中的表达;同时,行经皮肾穿刺活检供肾修整结束时、移植后7 d、1个月、6个月、1年或以上获取活检肾脏组织,用免疫组织化学方法检测活检组织中B7-2/CD28的表达情况。 结果与结论：移植后1,3 d内所有患者外周血中CD28+,CD4+/CD28+,CD8+/CD28+细胞比率均有显著下降(P < 0.05),一二周后恢复到术前水平;移植后7 d未发生急性排斥反应的患者肾脏组织B7-2阳性表达率显著上升(P < 0.05),1个月后下降至移植前水平(P > 0.05)。移植后发生急性排斥反应的患者外周血CD28+,CD4+/CD28+,CD8+/CD28+细胞比率及肾脏组织B7-2阳性表达率明显上升(P < 0.05),经抗排斥治疗1周后均好转。结果证实,在肾移植后出现急性排斥反应时,肾脏组织以及外周血中共刺激分子B7-2/CD28的表达上调与急性排斥反应的发生密切相关。       

慢性肾炎患者外周血T细胞亚群和共刺激分子的表达及其意义

为研究慢性肾炎患者外周血T细胞亚群和共刺激分子的表达特点及其在慢性肾炎免疫病理机制中的作用 ,本文采用免疫荧光标记和流式细胞仪分析 ,对 35例慢性肾炎患者外周血T淋巴细胞亚群和共刺激分子CD2 8、 4 1BB等的表达进行研究。结果表明 :(1)慢性肾炎患者T细胞亚群明显失衡 ,表现为CD4减少 ,CD8增加 ,CD4/CD8比值显著降低 ;(2 )共刺激分子CD2 8表达显著低于正常对照组 (CD2 8表达百分率分别为 45 95± 5 6 7和 6 6 42± 4 5 8,P <0 0 0 1) ,且CD4+ CD2 8+ T细胞和CD8+ CD2 8+ T细胞均显著减少。治疗后缓解期患者T细胞亚群失衡明显纠正 ,CD2 8+ T细胞 ,尤其是CD4+ CD2 8+ T细胞显著增多 ,而且CD4+ CD2 8+ T细胞数与患者的 2 4h尿蛋白定量呈负相关 (r= 0 47,P <0 0 1) ;(3)慢性肾炎患者共刺激分子 4 1BB在T细胞中的表达显著高于正常对照组 (表达百分率分别为 30 5 7± 8 12和 0 74± 0 2 8,P <0 0 0 1) ,治疗后的 4 1BB表达水平显著降低 ,而且 4 1BB异常高表达与CD8+ T细胞数呈正相关 (r=0 6 3,P <0 0 5 )。从而表明慢性肾炎外周血T细胞亚群失衡和T细胞活化所必需的共刺激分子CD2 8、 4 1BB异常表达 ,可能在慢性肾炎发生和病变进展中起着重要作用。     

支气管哮喘与PBMC上CD11a、CD18、CD44分子表达的关系

本文探讨 β整合素家族及CD44粘附分子在哮喘发病中的作用。采用流式细胞仪分别检测哮喘豚鼠外周血单个核细胞(PBMC )表面CD11a分子及哮喘患者PBMC表面CD18和CD44等分子的表达情况。结果 :(1)哮喘豚鼠PBMC表面CD11a分子表达明显高于对照组 (P <0 0 1) ,地塞米松可抑制CD11a表达 ;(2 )哮喘患者PBMC表面CD18、CD44表达较正常人明显增高 (P <0 0 1)。使细胞粘附分子参与了哮喘的病理生理过程 ,糖皮质激素可抑制细胞粘附分子表达 ,发挥抗炎作用。     

骨关节炎与免疫关联性初探

为了探讨免疫因素是否介导骨关节炎的发病 ,应用直接免疫荧光法检测了 6例晚期骨关节炎患者滑膜液中浸润淋巴细胞分化抗原的表达 ,同时用微量酶联免疫技术测定了这些患者滑膜液中IL 10、IL 12和sFasL的含量。结果显示关节滑膜液中的淋巴细胞以CD8+ 细胞为主 (6 7 0 %± 14 6 %) ,远远高于CD4+ 细胞 (15 0 %± 12 8%) ,两者相差显著 (P <0 0 1)。CD4+ /CD8+ 比值 <1。进一步分析表明其T细胞受体主要为αβ型TCR (6 4 0 %± 12 6 %)。滑膜液中IL 12含量 (2 0 3 84±49 2 )pg/ml高于IL 10 (37 8± 14 5 )pg/ml,有明显统计学差异 (P <0 0 1)。外周血中IL 10和IL 12的含量分别为 (4 3 37±14 2 )pg/ml和 (4 5 5 8± 10 6 )pg/ml。血清中sFasL含量较高 (15 3 90± 5 6 )pg/ml,而滑膜液中则很低 (<5pg/ml,P <0 0 1)。提示在骨关节炎的晚期CD8+ 淋巴细胞和IL 12增高可能参与了关节的免疫损伤。     

血栓性脑血管疾病患者治疗前后血小板活化膜表面糖蛋白检测及临床意义

目的 :探讨血栓性脑血管疾病患者治疗前后血小板活化标记物CD62 P,GPⅡb/Ⅲa的表达及其临床应用价值。方法 :采用流式细胞仪 (FCM )检测治疗前后血小板活化标记物CD62 P、GPⅡb/Ⅲa的表达。结果 :血栓性脑血管疾病患者治疗前血小板活化标志物CD62 P、GPⅡb/Ⅲa分别为CD62 P5 2 .19± 12 .3 7% ,GPⅡb/Ⅲa 77.98± 14 .2 2 % ,较正常对照组有显著性升高 (P <0 .0 1) ;治疗后CD62 P3 1.16± 17.43 % ,GPⅡb/Ⅲa 40 .71± 11.64 %较治疗前有显著性下降 (P<0 .0 1) ,但仍高于正常对照组 (P <0 .0 1)。结论 :血小板活化标志物CD62 P、GPⅡb/Ⅲa对血栓性脑血管疾病的诊断具有重要价值 ,为临床症状缓解后患者长期药物预防提供理论依据     

CD40L单克隆抗体对HSP患儿PBMC及单核细胞株THP-1产生炎症因子的影响

目的　观察CD4 0配体单克隆抗体 (CD4 0LMcAb)对HSP(亨诺 许兰紫癜 )患儿PBMC及单核细胞株THP 1产生炎症因子的影响。方法　采用细胞培养、流式细胞技术及ELISA法分别检测正常对照、过敏性紫癜患儿的PBMC及单核细胞株THP 1表达膜蛋白分子CD4 0L、CD4 0的阳性率、产生炎症因子IL 1、TNF α、IL 6水平以及CD4 0LMcAb加入细胞培养体系后上述指标的变化。结果　与正常比较 ,HSP患儿的PBMC表达CD4 0L[(8.2 6± 4 .15 ) % ,对照 (0 .5 4± 0 .5 8) % ]显著增高、CD4 0表达无差异 ;PBMC培养上清中炎症因子IL 1[(10 0 0 .4± 5 74 .5 )pg ml,对照 (2 4 6 .8± 2 0 7.1)pg ml]、TNF α[(978.7± 2 0 5 .8)pg ml,对照 (45 2 .4± 2 4 8.5 )pg ml]的水平也显著高于对照 ,CD4 0LMcAb可使增高的IL 1[(16 4 .7± 12 7.9)pg ml]、TNF α[(6 74 .7± 2 6 9.2 )pg ml]降至正常水平。THP 1自发表达CD4 0 ,低浓度产生IL 1、TNF α。与正常比较 ,HSP患儿的PBMC培养上清诱导其表达CD4 0 ,产生IL 1,TNF α增高 ,CD4 0LMcAb同样具有抑制THP 1表达CD4 0、分泌IL 1、TNF α的作用。结论　CD4 0LMcAb能抑制炎症因子的产生。     

重症肌无力患者外周血CD5~+B细胞和CD4~-CD8~-T细胞的变化

研究重症肌无力 (MG )患者外周血CD5 + B细胞和CD4 CD8 T细胞的变化 ,以探讨这两种细胞与MG的关系。采用流式细胞仪分析MG患者和对照组外周血中CD5 + B细胞和CD4 CD8 T细胞的频率 ,同时以ELISA方法检测这些患者的血清AchR、PsmR抗体水平。结果 :2 8例MG患者的CD5 + B细胞为 19 75 %± 10 8% ,高于对照组的 15 4 %± 9 6 7% (P <0 0 1) ;胸腺未切除MG患者的CD5 + B细胞为 2 2 31%± 7 4 7% ,显著高于对照组 (P <0 0 0 1) ;两种抗体阳性MG患者的CD5 + B细胞为 2 4 96 %± 13 1% ,显著高于对照组 (P <0 0 0 1) ;以上各组MG患者的CD4 CD8 T细胞与对照组均无显著区别 ;两种抗体阴性组的CD5 + B细胞和CD4 CD8 T细胞亦与对照组均无显著区别 ;两种抗体阴性组的CD5 + B细胞和CD4 CD8 T细胞亦与对照组无明显差异。本研究提示MG患者外周血的CD5 + B细胞频率增高 ,与胸腺切除与否以及突触前后膜抗体的阳性程度密切相关 ,而CD4 CD8 T细胞是否与MG有关还需进一步研究证实。     

大鼠心脏移植排斥反应过程中外周血CD28、CD40通路相关分子的变化

目的探讨CD28、CD40共刺激通路与排斥反应的关系,同时也为排斥反应的诊断寻找一种新的检测指标。方法采用大鼠异位心脏移植模型,用免疫组化方法动态检测外周血单核细胞（PBMC）CD28、CTLA4、CD40及CD40L分子的表达。结果在0～4级排斥反应中,外周血细胞CD28分子阳性表达率在各组间的差异无统计学意义。外周血细胞表达CTLA4分子的阳性率随排斥反应增强而升高（P〈0.01）。CD40及CD40L在PBMC中的表达强度也随排斥反应的分级逐渐增强（P〈0.01）。结论外周血CTLA4、CD40及CD40L分子的表达与排斥反应有密切关系,动态检测这些分子有助于对排斥反应状态的评价。     

Reduced CD40L expression on ex vivo activated CD4+ T-lymphocytes from patients with excellent renal allograft function measured with a rapid whole blood flow cytometry procedure

BACKGROUND: The CD40-CD40L (CD154) costimulatory pathway plays a critical role in the pathogenesis of kidney allograft rejection. In renal transplant biopsies, CD4+CD40L+ graft-infiltrating cells were detected during chronic rejection in contrast to acute rejection episodes. Using a rapid noninvasive FACS procedure, we were able to demonstrate CD40L upregulation in peripheral blood of patients with chronic renal allograft dysfunction. MATERIALS AND METHODS: Whole blood from recipients of renal allografts was stimulated with PMA and ionomycin and measured by flow cytometry. Patients were assigned to three groups based on transplant function. Group 1: 26 patients with excellent renal transplant function; group 2: 28 patients with impaired transplant function; group 3: 14 patients with chronic allograft dysfunction and group 4: 8 healthy controls. RESULTS: The median percentage +/- SEM of CD4+/CD40L+ cells stimulated ex vivo at 10 ng/ml PMA was as follows: group 1: 28.3 +/- 4.1%; group 2: 18.4 +/- 2.4%; group 3: 50.1 +/- 5.0% and group 4: 40.4 +/- 3.4%. Subdivisions of groups 2 and 3 resulted in different CD40L expression patterns. Patients with increased serum creatinine since the initial phase after transplantation (groups 2a and 3a) revealed a higher percentage of CD4+CD40L+ cells than patients showing a gradual increase over time (groups 2b and 3b). Consequently, patients of group 3a exhibited a significantly reduced transplant function compared with those of group 3b. CONCLUSION: After PMA + ionomycin stimulation, patients with excellent kidney graft function displayed significantly reduced expression of CD40L surface molecules on CD4+ cells early after transplantation. Those with a chronic dysfunction of the renal graft showed significantly more CD4+ cells expressing CD40L compared to the other transplanted groups. These results demonstrate that the percentage of CD4+CD40L+ cells stimulated ex vivo in peripheral blood may be a valuable marker for chronic allograft nephropathy.     

大鼠移植慢性排斥组织中CD40和CD40L表达研究

目的：观察大鼠移植肾慢性排斥肾组织中CD40／40L的原位表达特点。以期阐明CD40／CD40L共刺激通路在移植肾脏慢性排斥反应中的作用。方法：共分3个实验组：即同种异体移植不用药对照组、用品系移植组、同种异体移植CSA治疗组。用SP免疫组织化学方法对移植肾脏组织CD40／CD40L表达进行观察，并结合肾间质中浸润的炎性细胞CD3^ 和CD68^ 细胞数进行分析。结果：慢性排斥肾组织中CD40／CD40L表达分布不同，间质淋巴细胞以表达CD40为主，CD40L表达肾实质细胞表达为主。慢性排斥移植肾组织间质CD40^ 细胞数与CD3^ 、CD68^ 细胞数密切相关；CD40L^ 细胞数与CD3^ 细胞数呈正相关，与CD68^ 细胞数无相关性.结论：CD40／CD40L共刺激通路可能在移植肾慢性排斥的发生、发展过程中起重要作用。     

Decreased humoral antibody episodes of acute renal allograft rejection in recipients expressing the HLA-DQβ1*0202 allele

The present investigation was designed to show the effect of human leukocyte antigen (HLA) class II molecular allelic specificities in the recipient on the induction of humoral antibody rejection, identified by C4d peritubular capillary staining, as well as specific antibody identified by Luminex technology. Major histocompatibility complex (MHC) class II molecules are expressed on dendritic cells, macrophages, and B lymphocytes and they present antigenic peptides to CD4 positive T lymphocytes. Human renal peritubular and glomerular capillaries express class II MHC molecules upon activation. Expression of class II molecules on renal microvascular endothelial cells exposes them to possible interaction with specific circulating antibodies. We hypothesize that HLA-DQβ1*0202 expression in recipients decreases the likelihood of antibody-mediated renal allograft rejection. We found that 80% (=25) of DQ2 positive haplotype recipients failed to induce humoral antibody renal allograft rejection and 20% (n=25) of DQ2 positive haplotype recipients induced humoral antibody renal allograft rejection (p=0.008). By contrast, 48% (n=46) of DQ2 negative haplotype recipients failed to induce a humoral antibody component of renal allograft rejection and 52% (n=46) of DQ2 negative haplotype recipients induced humoral antibody-mediated renal allograft rejection. Our results suggest that recipients who express the DQβ1*0202 allele are less likely to induce a humoral antibody component of acute renal allograft rejection than are those expressing DQ1, DQ3, or DQ4 alleles. DQβ1*0202 allele expression in recipients could possibly be protective against acute humoral allograft rejection and might serve as a future criterion in recipient selection and in appropriate therapy for acute renal rejection episodes.     

尿CD54+淋巴细胞在肾移植急性排斥反应中的变化

背景：正常肾脏、肾小管上皮和血管内皮细胞仅有少量CD54表达,当发生急性排斥反应时,肾小管上皮细胞和血管内皮细胞CD54表达明显增加,同时大量白细胞浸润;间质浸润细胞和肾小管上皮细胞CD54表达增加。 目的：探讨流式细胞仪检测尿CD54⁺淋巴细胞对移植肾急性排斥反应的诊断价值。 方法：来自解放军成都军区总医院的肾移植后恢复正常者(n=18)、出现急性排斥反应者(n=8)、移植肾功不全者(n=9)以及健康志愿者(n=10)。流式细胞仪比较各组移植前后尿液中CD54⁺淋巴细胞比率变化。 结果与结论：尿CD54⁺淋巴细胞在肾移植患者出现排斥反应时明显增加(P < 0.01),抗排斥治疗后逐渐下降。移植肾功能正常者和移植肾功不全者CD54轻度升高。提示尿液中CD54⁺淋巴细胞水平能准确反映肾移植物移植后患者的免疫状态,可作为肾移植后急性排斥反应的特异标志。     

肾移植后外周血CD4+及CD8+T细胞亚群计数的临床意义

背景：临床上常以流式细胞检测受者外周血CD4、CD8细胞比值来揭示与排斥或感染相关的关系。 目的：探讨肾移植后排斥或感染时外周血CD4⁺及CD8⁺T细胞(简称CD4和CD8细胞)亚群计数的变化和意义。 方法：应用流式细胞仪检测肾移植121例受者CD4、CD8细胞数进行检测。根据入院病情将患者分为移植后正常组、急性排斥组、肺部感染组进行观察。 结果与结论：移植后正常患者和急性排斥患者相比,CD4、CD8细胞数差异均无显著性意义(P > 0.05)。肾移植后肺部感染患者CD4、CD8细胞数则均显著低于移植后正常组(P < 0.001)。当感染控制、症状改善时,CD4、CD8细胞数显著升高 (P < 0.001)。说明肾移植后CD4和CD8细胞计数可以作为免疫状态的参考,其对于感染的参考价值大于排斥,动态观察分析有助于指导治疗。     

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR-P1 and Reduction of CD43

Monocytes and macrophages mediate cytotoxicity after appropriate activation and thus represent effectors secondary to T lymphocytes and natural killer (NK) cells. However, very little is known about the role of activated monocytes in organ allograft rejection. In this study, isogeneic (LEW to LEW) and fully allogeneic (DA to LEW) rat kidneys were grafted to bilaterally nephrectomized recipients. Four days after transplantation a comprehensive sample of leucocytes was recovered by perfusion of the recipients' vasculature with phosphate-buffered saline containing EDTA (PBS/EDTA). Monocytes were enriched by density gradient centrifugation and their physical parameters and immunophenotype were investigated by flow cytometry in comparison with untreated, specified pathogen-free (SPF) LEW rats. Isotransplantation and allotransplantation of kidneys dramatically increased the absolute number of intravascular monocytes in the recipient. Analysis of NKR-P1 (CD161), CD4, CD62L, CD43, CD11a, CD18 and MHC class II expression identified at least two monocyte populations in all experimental groups. In graft recipients it was evident that activated monocytes were able to express and upregulate NKR-P1 and CD8, which have not been detected in these cells to date. If activated monocytes utilize NKR-P1 and CD8, by analogy to NK cells and lymphocytes these cells may be endowed with additional pathways to upregulate cytolytic functions and effect allograft damage.     

CD44/CD70 blockade and anti-CD154/LFA-1 treatment synergistically suppress accelerated rejection and prolong cardiac allograft survival in mice

Current treatments that are efficient in controlling effector T cell responses to allografts have limited efficacy on the accelerated rejection mediated by memory T cells. Effective targeting of alloreactive memory T cells may therefore be explored to improve therapeutic approaches towards solving this problem. In this study, we investigated the synergistic effect of CD44/CD70 blockade and anti-CD154/LFA-1 treatment on the accelerated rejection mediated by memory T cells. While CD44/CD70 blockade had limited effects on the alloresponses of effector T cells in vivo, it diminished the expansion of both CD4(+) and CD8(+) memory T cells in recipients adoptively transferred with donor-sensitized T cells. In combination with anti-CD154/LFA-1 treatment, CD44/CD70 blockade significantly prolonged cardiac allograft survival in adoptive transfer recipients. We demonstrated that treatment with the combination of all four antibodies (anti-CD154/LFA-1/CD44/CD70) inhibited accelerated rejection by markedly suppressing the alloresponses of effector and memory T cells and reducing the number of graft-infiltration lymphocytes in adoptive transfer recipients. Meanwhile, CD44/CD70 blockade and anti-CD154/LFA-1 treatment synergically enhanced regulatory T cells (Tregs) by increasing the proportion of splenic Tregs and the expression of IL-10 in these recipients. Our findings contribute to the potential design of therapies for accelerated allograft rejection.     

同种异体移植肾组织中CD80和CD86表达的观察

目的观察同种异体肾移植肾组织中CD80和CD86的表达,以探讨其在急性肾移植细胞性排异反应中可能的致病作用。方法以正常肾组织(NC组)为对照,采用免疫组织化学方法观察急性细胞性排异反应组(ACR组),无急性细胞性排异反应组(N-ACR组)肾组织中CD80和CD86的表达及肾间质中浸润CD4+和CD8+淋巴细胞数。结果ACR组肾小管上皮细胞的CD80和CD86表达较N-ACR组增高,其肾间质中CD4+和CD8+淋巴细胞数也较N-ACR组和NC组明显增高,同时N-ACR组肾间质的CD4+和CD8+表达较NC组明显增高。结论肾小管上皮细胞作为抗原提呈细胞参与了同种异体肾移植急性细胞性排异反应过程。